James M. Falko

Benign Parotid Enlargement in Bulimia

Bulimia is an episodic compulsive urge to overeat often followed by recurrent attempts to lose weight by self-induced vomiting. Seven young women with this eating disorder and associated benign bilateral painless parotid enlargement are described. The glandular swelling was generally intermittent, with parotid enlargement usually developing 2 to 6 days after a binge overeating episode had stopped. Several had hypokalemic alkalosis and a moderate elevation in serum amylase levels. None had clinical evidence of pancreatitis, and a parotid gland biopsy in one patient was normal. The clinician should be alerted to the association of benign parotid enlargement with this syndrome.

Effect of a Community-Based Weight Management Program on Weight Loss and Cardiovascular Disease Risk Factors

Objective: The purpose of our retrospective database analysis was to describe and evaluate the outcomes of a weight loss intervention in a community medical wellness center.

Concomitant insulin and sulfonylurea therapy in patients with type II diabetes: Effects on glucoregulation and lipid metabolism

Recent evidence suggests concomitant insulin and sulfonylurea therapy has a theoretical potential in the management of type II diabetes mellitus. In a long-term double-blind, randomized placebo-controlled study of combination therapy, serum glucose, C-peptide, total cholesterol, triglyceride, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol concentrations were evaluated in insulin-treated patients with poorly controlled, type II diabetes mellitus after addition of either glyburide (n = 10) or placebo (n = 12). Oral glucose tolerance testing was performed at weeks 0, 4, and 16. Clinical characteristics and glycemic control (fasting blood glucose and glycosylated hemoglobin values) were similar at week 0 in both groups. The placebo group had no change in any metabolic parameter throughout the study period. At week 4, glyburide significantly lowered fasting blood glucose and integrated glucose areas (p less than 0.01) compared with values at week 0 (fasting blood glucose 225 +/- 20 versus 286 +/- 27 mg/dl, p less than 0.02). Mean fasting, stimulated, and integrated C-peptide levels were significantly higher (p less than 0.02) at week 4 versus week 0. At week 16, mean fasting blood glucose values remained significantly lower compared with baseline values (252 +/- 25 versus 286 +/- 27 mg/dl, p less than 0.05). Glycosylated hemoglobin levels decreased significantly (p less than 0.05) at weeks 4 to 16 compared with the baseline values. Although glucose responses and integrated areas were no different after oral glucose tolerance testing, fasting and stimulated C-peptide levels were significantly higher (p less than 0.05) at week 16 versus week 0. Lipid and lipoprotein levels remained unchanged. In summary, combination therapy consisting of glyburide and insulin moderately improved glucose control in type II diabetes mellitus at the end of four weeks. Despite significantly lower fasting serum glucose and glycosylated hemoglobin levels after 16 weeks, combination treatment did not normalize glycemic control. Glucose tolerance decreased further after 16 weeks despite persistence of increased endogenous insulin secretion. The role of the combination therapy in the long-term care of patients with type II diabetes mellitus needs further investigation.

Diabetogenic effect of pentamidine: In vitro and in vivo studies in a patient with malignant insulinoma

Pentamidine can cause hypoglycemia followed by hyperglycemia. The mechanism of this biphasic response is not known but has been reported to be similar to that of streptozotocin and N-3-pyridyl-N-p- nitrourea (Vacor). Pentamidine (4 mg/kg per day for 12 days) was used in a patient with malignant insulinoma after several unsuccessful debulking procedures and chlorozotocin therapy. Mean glucose and immunoreactive insulin levels (+/- SEM) before and after therapy were 80 +/- 40 mg/dl versus 70 +/- 50 mg/dl and 216 +/- 12 microU/ml versus 198 +/- 22 microU/ml, respectively. These were not significantly different. The patients five-month-old malignant insulinoma monolayer cell culture was incubated with pentamidine (60 micrograms/ml) in the presence or absence of supplemented stimulatory medium consisting of glucose (300 mg/dl) and theophylline (20 micrograms/ml). Chloroquine (60 micrograms/ml) was added to inhibit lysosomal degradation of immunoreactive insulin. Aliquots of media for immunoreactive insulin determination were obtained at 30 minutes, 20 hours, 72 hours, and three weeks. The cells were examined by high-power light microscopy at each time interval. At 30 minutes, pentamidine alone caused passive release of immunoreactive insulin, 23 percent higher than control (p less than 0.01). Stimulatory medium increased immunoreactive insulin 45 percent greater than control (p less than 0.01). Pentamidine plus stimulatory medium had no additive effect on immunoreactive insulin released within 30 minutes. At the end of 20 hours, immunoreactive insulin was no different with pentamidine and/or stimulatory medium. However, the addition of chloroquine increased immunoreactive insulin by 35 percent above the medium with pentamidine and stimulatory medium (p less than 0.01). At 72 hours, pentamidine suppressed immunoreactive insulin by 100 percent in all the media, irrespective of the presence or absence of stimulatory medium and/or chloroquine. At the end of three weeks, there was 50 percent suppression of immunoreactive insulin in the control medium, but pentamidine again completely suppressed immunoreactive insulin. High-power microscopy demonstrated intact cells in the control medium, whereas no cell structure could be detected in the media containing pentamidine at three weeks. In summary, pentamidine had no acute in vivo effect in a patient with malignant insulinoma. However, when used in an in vitro monolayer system, pentamidine caused (1) acute immunoreactive insulin release followed by inhibition of immunoreactive insulin secretion and (2) cytolysis of human malignant insulinoma cells in vitro.

Cardiac rehabilitation is associated with an improvement in C-reactive protein levels in both men and women with cardiovascular disease.

PURPOSEnInflammation is involved in the development of atherosclerotic plaque. The most studied indicator of inflammation in coronary heart diseases (CHD) is C-reactive protein (CRP) which has prognostic significance in those with CHD. The purpose of this study is to evaluate the effect of participation in cardiac rehabilitation (CR) on this marker of vascular inflammation, CRP.nnnMETHODSnWe analyzed CRP levels in 172 patients with CHD who participated in a CR program.nnnRESULTSnMen and women in CR demonstrated significant improvement in body mass index (-0.35, P = .002), exercise capacity (METs 1.8, P < .0001), HDL-C (1.8, P = .003), and CRP (-3.1, P = .003). The improvement in CRP was not significantly different based on age or the presence of metabolic syndrome.nnnCONCLUSIONnParticipation in CR was associated with a marked improvement of cardiac risk factors and appears to independently decrease the level of CRP regardless of gender, age, or presence of metabolic syndrome.

Type III hyperlipoproteinemia: Rise in high-density lipoprotein levels in response to therapy☆

Abstract The experience of the Washington University Lipid Research Center in the treatment of type III hyperlipoproteinemia is reported. Six women and seven men were prescribed a type III diet and/or clofibrate over periods of two to eight months. Mean total plasma cholesterol and triglyceride levels declined by 51 and 74 per cent, respectively, whereas mean levels of high-density lipoprotein (HDL) cholesterol rose from 34 to 50 mg/dl (p levels and compositions of the low- and high-density lipoproteins were affected by therapy. Levels of cholesterol and triglycerides in the d

Lipoprotein analyses in varying degrees of glucose tolerance: Comparison between non-insulin-dependent diabetic, impaired glucose tolerant, and control populations☆

Atherosclerosis is the major cause of death in diabetic patients. Lipoproteins and lipids are frequently altered in non-insulin-dependent diabetes. These lipoprotein alterations are of interest because of their possible role in the origin of the accelerated atherosclerosis found in diabetes. Because of the link between lipoproteins and diabetes, serum lipids and lipoproteins were measured in 215 middle-aged patients (107 female, 108 male) with varying degrees of glucose tolerance: control subjects, subjects with impaired glucose tolerance (IGT), and patients with non-insulin-dependent diabetes mellitus (NIDDM). In male subjects, levels of fasting total triglycerides were significantly greater in those with NIDDM compared with control subjects. In female subjects, fasting total cholesterol levels were significantly greater in NIDDM compared with IGT. Both high-density lipoprotein (HDL) cholesterol and HDL2 cholesterol values were significantly lower in both sexes with NIDDM compared with control subjects. Low-density lipoprotein (LDL) cholesterol levels were elevated in the male subjects with IGT. No differences in HDL cholesterol or its subfractions were seen in both sexes with IGT compared with control subjects. Bivariate analyses showed that the reduced HDL cholesterol and HDL subfraction levels were most closely associated with both total triglycerides and weight. This study shows that reduced HDL cholesterol and HDL2 cholesterol levels occur in NIDDM, whereas persons with impaired glucose tolerance do not have the dramatic alterations in HDL levels.

Combination insulin/glyburide therapy in type II diabetes mellitus: Effects on lipoprotein metabolism and glucoregulation

A randomized double-blind, placebo-controlled trial of insulin plus glyburide was carried out in 22 insulin-treated patients with poorly controlled type II diabetes mellitus. Glycemic control and lipoprotein responses were assessed for 16 weeks. Oral glucose tolerance testing was performed at weeks 0, 4, and 16. Clinical characteristics and glycemic control were similar at week 0 in the placebo/insulin group (n = 12) and the glyburide/insulin group (n = 10). Throughout the study, the dose of insulin was fixed. The placebo group had no change in any metabolic parameter throughout the protocol period. After four weeks, glyburide significantly lowered fasting blood glucose and integrated glucose areas (p less than 0.01) after oral glucose testing compared with week 0 (fasting blood glucose 225 +/- 20 mg/dl versus 286 +/- 27 mg/dl, p less than 0.02). Associated with this were mean fasting, stimulated, and integrated C-peptide levels that were significantly higher (p less than 0.02) at week 4 versus week 0. After 16 weeks, mean fasting blood glucose remained significantly lower compared with baseline values (252 +/- 25 mg/dl versus 286 +/- 27 mg/dl, p less than 0.05). Glycosylated hemoglobin (hemoglobin A1c) levels decreased significantly (p less than 0.05) at weeks 4 to 16 compared with the baseline value. Although integrated areas were no different after oral glucose, fasting and stimulated C-peptide levels were significantly higher (p less than 0.05) at week 16 versus week 0. Total cholesterol, triglycerides, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol did not change during the study. After the code was broken, comparisons were made between those with response to combination therapy (reduction of fasting blood glucose by at least 50 mg/dl or fasting blood glucose of 140 mg/dl or less at the end of the first week of treatment that persisted for four consecutive weeks) and those without response. Baseline clinical and laboratory characteristics were identical in both groups. Mean fasting and stimulated serum C-peptide levels after oral glucose, however, were significantly higher in the patients with response at week 4 compared with the patients without response. The mean maximal incremental C-peptide level was 1.50 +/- 0.19 ng/ml at week 0 in the patients with response compared with 0.67 +/- 0.28 ng/ml in the patients without response (p less than 0.01). Lipoproteins were not different in the two groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Dietary Treatment of Type V Hyperlipoproteinemia Fails to Normalize Low Levels of High-Density Lipoprotein Cholesterol

Excerpt Recent epidemiologic and experimental data suggest that high-density lipoproteins may protect against the development of atherosclerosis (1, 2). Cross-sectional population studies have show...

Decreased Serum C-Peptide/Insulin Molar Ratios After Oral Glucose Ingestion in Hyperthyroid Patients

Since C-peptide/immunoreactive insulin (IRI) molar ratios may reflect hepatic extraction of insulin, we measured simultaneous serum glucose, IRI, and C-peptide levels during fasting and 30, 60, 90, 120, and 180 min after 75 g of oral glucose in 10 hyperthyroid patients and 10 age- and weight-matched controls. Mean fasting serum glucose and IRI levels were significantly higher in the hyperthyroid versus control subjects (glucose: 4.9 ± 0.3 mmol/L versus 4.36 ± 0.11 mmol/L, P < 0.01; IRI: 0.10 ± 0.02 pmol/ml versus 0.05 ± 0.01 pmol/ml; P < 0.025). After glucose, mean serum glucose levels were significantly higher in the hyperthyroid versus control subjects at all times studied except for 180 min (P < 0.01). Mean IRI levels were significantly higher at all times studied including 180 min (P < 0.01). Mean fasting C-peptide levels were significantly greater in the hyperthyroid patients compared with the controls (1.2 ± 0.25 pmol/ml versus 0.62 ± 0.09 pmol/ml; P < 0.025). After oral glucose, mean C-peptide levels were significantly higher (P < 0.025) in the hyperthyroid compared with control subjects at 30–60 min but not at 90–180 min. Molar ratios of C-peptide/IRI were significantly lower (P < 0.05) in the hyperthyroid versus control subjects at all times studied except fasting. In summary, glucose intolerance and hyperinsulinism occur in hyperthyroidism. In addition, C-peptide/IRI molar ratios are reduced after oral glucose ingestion.